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Richard A. Flavell

Researcher at Yale University

Publications -  1389
Citations -  223064

Richard A. Flavell is an academic researcher from Yale University. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 231, co-authored 1328 publications receiving 205119 citations. Previous affiliations of Richard A. Flavell include National Institute for Medical Research & University of Michigan.

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Expression of Interleukin-10 in Intestinal Lymphocytes Detected by an Interleukin-10 Reporter Knockin tiger Mouse

TL;DR: The intestine is highlighted as a unique site for induction of IL-10-producing T cells, which play a critical role in the regulation of inflammation in the gut.
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Epithelial IL-18 Equilibrium Controls Barrier Function in Colitis.

TL;DR: It is shown that IL-18 is critical in driving the pathologic breakdown of barrier integrity in a model of colitis, and the mechanism of goblet cell dysfunction that underlies the pathology of ulcerative colitis is informed on.
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Cutting Edge: TGF-β Inhibits Th Type 2 Development Through Inhibition of GATA-3 Expression

TL;DR: It is demonstrated that TGF-β inhibits GATA-3 expression in developing Th cells, which is a major mechanism of inhibition of Th2 differentiation by T GF-β as ectopic expression of Gata-3 in developing T cells overcomes the ability of TGF -β to inhibit Th 2 differentiation.
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Does Toll-like receptor 3 play a biological role in virus infections?

TL;DR: The results indicate that TLR3 is not universally required for the generation of effective antiviral responses because the absence ofTLR3 does not alter either viral pathogenesis or impair host's generation of adaptive antiviral response to these viruses.
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Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis

TL;DR: These studies establish novel regulatory roles for BRP-39/YKL-40 in the initiation and effector phases of Th2 inflammation and remodeling and suggest that these proteins are therapeutic targets in Th2- and macrophage-mediated disorders.